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Copper Deficiency Caused by Excessive Alcohol Consumption Shunichi Shibazaki,1 Shuhei Uchiyama,2 Katsuji Tsuda,3 Norihide Taniuchi4

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Copper Deficiency Caused by Excessive Alcohol Consumption Shunichi Shibazaki,1 Shuhei Uchiyama,2 Katsuji Tsuda,3 Norihide Taniuchi4 Findings that shed new light on the possible pathogenesis of a disease or an adverse effect BMJ Case Reports: first published as 10.1136/bcr-2017-220921 on 26 September 2017. Downloaded from CASE REPORT Copper deficiency caused by excessive alcohol consumption Shunichi Shibazaki,1 Shuhei Uchiyama,2 Katsuji Tsuda,3 Norihide Taniuchi4 1Department of Emergency SUMMARY managed by crawling. A day before his visit to our and General Internal Medicine, Copper deficiency is a disease that causes cytopaenia hospital, his behaviour became unintelligible, and Hitachinaka General Hospital, and neuropathy and can be treated by copper he was brought to our hospital by ambulance. He Hitachinaka, Ibaraki, Japan supplementation. Long-term tube feeding, long-term had a history of hypertension and dyslipidaemia 2Department of General Internal total parenteral nutrition, intestinal resection and and took amlodipine and rosuvastatin. He has no Medicine, Tokyo Bay Urayasu history of surgery and he did not take zinc medica- Ichikawa Medical Center, ingestion of zinc are known copper deficiency risk Urayasu, Chiba, Japan factors; however, alcohol abuse is not. In this case, a tion or supplementation. 3Department of Nephrology, 71-year-old man had difficulty waking. He had a history Vital signs were the following: blood pressure Suwa Central Hospital, Chino, of drinking more than five glasses of spirits daily. He was 96/72 mm Hg, pulse 89/min, body temperature Nagano, Japan well until 3 months ago. A month before his visit to our 36.7°C, respiration rate 15/min at time of visit. 4Department of hospital, he could not eat meals but continued drinking. He lost consciousness and could not understand Gastroenterology and Internal He had macrocytic anaemia on admission. Copper where he was or respond to instructions. His ocular Medicine, Suwa Central and ceruloplasmin levels were markedly low, and we conjunctiva was yellow tinged and he had a flap- Hospital, Chino, Nagano, Japan diagnosed copper deficiency. There were no other known ping tremor. He had an abdominal bulge and no risk factors for copper deficiency. After he began drinking knock pain around his liver. He had brown diar- Correspondence to rhoea, not tarry stool. He was unable to stand up Dr Shunichi Shibazaki, cocoa as a copper supplement, the anaemia ameliorated sn1. shibazaki@ gmail. com and he was able to walk. This is the first report showing to both knees. Babinski reflection was positive. He alcohol abuse as a risk factor for copper deficiency. was uncooperative with our physical examination, Accepted 12 September 2017 and as such, a detailed neurological examination including serial exams was not possible. copyright. BACKGROUND INVESTIGATIONS Copper deficiency is a disease that causes blood cell Blood tests revealed a white blood cell count of abnormalities such as anaemia and leucopaenia1, 5190/μL without abnormal fractionation. His and neurological symptoms such as neuropathy, haemoglobin (Hb) was 7.8 g/dL (normal range myelopathy and vision loss.2 It needs to be differ- 13.5–17.6 g/dL), mean corpuscular volume was entiated from vitamin B 12 deficiency. Although the 107.4 fl (normal range 83–93 fl), reflecting macro- http://casereports.bmj.com/ precise frequency is unknown, primary copper defi- 4 cytic anaemia. Platelet count was 11.7×10 /μL ciency is relatively rare because copper is univer- 4 4 3 (normal range 13.1×10 -36.2×10 /μL), reflecting sally included in the diet. Therefore, it should be mild thrombocytopaenia. Aspartate aminotrans- suspected when the patient has a known risk factor. ferase was 477 IU/L (normal range 7-97 IU/L), Current known risk factors include special nutri- 4 alanine aminotransferase was 155 IU/L (normal tional conditions such as long-term tube feeding 5 range 6–43 IU/L), blood urea nitrogen was 26.7 and long-term total parenteral nutrition , gastro- mg/dL (normal range 10–20 mg/dL), creatinine intestinal problems such as postgastrectomy6 and 7 2.41 mg/dL (normal range 0.6–1.0 mg/dL), that is, postobesity surgery and other conditions, such as liver and kidney dysfunction were also observed. ingestion of zinc.8 There are also several copper 9 Blood glucose level was normal (137 mg/dL). on 26 September 2021 by guest. Protected deficiency case reports of unknown causes, , which Ammonia level increased up to 166 μg/dL (normal suggests that there are other risk factors. Currently range 30–80 μg/dL). His serum ferritin also signifi- in the literature, there are no case reports of alcohol cantly increased up to 9506 ng/mL (normal range abuse as a risk for copper deficiency. We experi- 39.4–340 ng/mL). C-reactive protein was 5.89 enced a case of copper deficiency due to alcohol mg/dL (normal range 0.0–0.3 mg/dL). However, abuse without other known risk factors. urinary white blood cells and bacterial urine were negative, thus excluding pyelonephritis. In addi- CASE PRESENTATION tion, ascites had no bacteria, while white blood A 71-year-old man was a long-term alcoholic that cell count in ascites was 32/μL, thus also excluding drank more than five glasses of spirits daily. Begin- spontaneous bacterial peritonitis. The following T o cite: Shibazaki S, ning 3 months ago, he began to eat less at meals data are reference values because these blood tests Uchiyama S, Tsuda K, et al. that consisted mostly of raw fish and meat and were investigated after vitamin ingestion at the BMJ Case Rep Published Online First: [please continued to drink alcohol. However, he had no emergency department; serum vitamin B1 91 ng/ include Day Month Year]. other problems in daily life. One month ago, he mL (normal range 24-66 ng/mL) and serum vitamin doi:10.1136/bcr-2017- could no longer eat meals but continued drinking. B12 >1500 pg/mL (normal range 180-914 pg/mL). 220921 At about this time, he became unable to walk and Prothrombin time (PT) was 16.5 s (normal range Shibazaki S, et al. BMJ Case Rep 2017. doi:10.1136/bcr-2017-220921 1 Findings that shed new light on the possible pathogenesis of a disease or an adverse effect BMJ Case Reports: first published as 10.1136/bcr-2017-220921 on 26 September 2017. Downloaded from OUTCOME AND FOLLOW-UP Serum copper and ceruloplasmin recovered rapidly, serum ferritin declined and blood cell count recovered after just a few days of drinking cocoa. His delirium also disappeared rapidly from the day after starting cocoa. Moreover, activity of daily life recovered rapidly (figure 1). Because he became cooperative with medical treatment, we used diuretics and BCAA sequen- tially. Eventually, he could walk on his own and was discharged on the 74th day and was ambulatory. The blood cells subsequently recovered: Hb 14.3 g/dL, however, Babinski reflexion remained positive 4 months after the start of copper supplementation. He continued abstinence after being discharged from our hospital and has had no relapse after 2 years of follow-up. DISCUSSION This is the first case report clinically, suggesting that excessive alcohol consumption can be a risk factor for copper deficiency. Copper is an essential element in the body, absorbed from the jejunum to duodenum,10 and it spreads throughout the body via the liver. It acts as a coenzyme for many enzymes, and in particular, plays an important role in the bone marrow and nerve system.11 Therefore, copper deficiency can result in blood cell abnormalities such as various types of anaemia (microcytic, normocytic, macrocytic anemia) and leucopenia1, and neurologic Figure 1 Clinical course of this case. Initially, symptoms did not symptoms such as neuropathy, myelopathy, and vision loss2. In improve with multiple treatments. However, it improved dramatically particular, it is important to differentiate this from vitamin B12 with copper supplementation via cocoa. ADL, activity of daily life; BCAA, deficiency because the phenotypes are similar. Copper supple- branched chain amino acid; Hb, haemoglobin; Ret, reticulocyte. mentation recovers blood cell abnormalities favourably.3 For neurological symptoms, however, the recovery is partial, and it copyright. is thought that neurological symptoms will become irreversible 11–14 s), PT% was 51.9% (normal range 80–120%). Head CT 12 revealed no abnormality, however, abdominal CT showed an if treatment is delayed. Therefore, it is important to diagnose advanced fatty liver and a massive amount of ascites. copper deficiency and start treatment early. Since he ramped and was uncooperative with our investiga- Copper deficiency may be overlooked. Although the exact tion, it was impossible to conduct a detail examination such as frequency of copper deficiency is unknown, primary copper deficiency is considered relatively rare as copper is included in with upper gastrointestinal endoscope to rule out gastrointes- 3 13 tinal bleeding. MRI of the spine and brain to confirm the cause most diets. Typically, clinician awareness is low, which makes http://casereports.bmj.com/ of being unable to walk was also not possible. correct diagnosis difficult. Generally, we suspect copper defi- ciency if the patient has a known risk factor. Known risk factors TREATMENT include special nutritional conditions such as long-term tube feeding4 and long-term parenteral nutrition5 or gastrointestinal Initially, we suspected vitamin B12 deficiency with hepatic 6 7 encephalopathy and prerenal renal failure. Therefore, intrave- problems such as postgastrectomy and postobesity surgery or other conditions, such as zinc intake.8 There are several nous vitamin B12 supplementation (more than 1000 µg daily), 9 branched chain amino acid (BCAA) administration and replace- case reports about copper deficiency of unknown cause. This ment fluid were administered. Lactulose was not used because suggests that clinically there may be other risk factors. he was not constipated but rather had diarrhoea.
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